To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Paraoxonase (PON), an enzyme, is a key process in the pathophysiology of atherosclerosis.
We aim to investigate the variations of PON1 activity in Tunisian bipolar I patients treated with thymoregulators.
Patients and methods
Our study included 78 patients with bipolar I disorder, diagnosed according to the DSM-IV, and 64 controls aged 35.97±11.55 years and 36,31±18.26 years respectively. 41 patients were treated by valproic acid, 16 under carbamazepine and 21 under lithium. PON1 activity was determined by kinetic methods using Konelab 30 equipment.
Compared to controls, patients treated by thymoregulators had a significantly lower paraoxonase activity (p=0.004). Furthermore, PON1 was significantly correlated with c-HDL values (r=0.5612; P< 0.001). The lowest PON1 levels were noted in patients treated with lithium (150±94UI/L) and the highest levels were showed in those under carbamazepine (260±185UI/L), but this difference was not significant. In patients under lithium, we showed that this parameter was significantly lower when illness duration was more than 12 years, the lithium posology exceeds 1000 mg/day and the lithium plasmatic concentrations were more than 0.54 mmol/L. However, there was no significant difference among gender, age, cigarette smoking and alcoholic beverage.
Bipolar patients had a significant decrease in PON1 activity that contributes to increased risk of cardiovascular diseases. This perturbation could be related to treatment with thymoregulators and particularly lithium. Therefore, such patients should require specific care and clinics should track the effects of treatment on physical and biological parameters, and should facilitate access to appropriate medical care.
This study aimed to evaluate the interference of tobacco smoke on immunochromatography assay for urinary benzodiazepines detection and the interest of two biological markers and smoking status parameters as predictive factors of false results.
Our study included 256 voluntary subjects (143 passive smokers and 113 smokers). Cotinine was measured by homogenous immunoenzymatic assay and SCN- by selective electrode. Urinary drugs were detected by immunochromatographic assay. A positive result is completed by an analytical method with an immunometric assay.
False positive results for benzodiazepines are significantly more frequent in smokers compared with passive smokers (90.2% Vs 22.4%, p< 10-3). For smokers, the number of cigarettes was significantly higher in subjects with falsely positive results for benzodiazepines compared with subjects with negative results (32 ± 11 Vs 20 ± 10; p= 0.04). Between these two groups, we established a significant difference for urinary cotinine (345 ± 211 Vs 117 ± 54 μg/μmol; p< 10-3) and for plasma SCN- (101.6 ± 3.4 Vs 98.8 ± 2.1μmol/L; p=10-3). Urinary cotinine and consumption duration present the highest values of AUC of the ROC curves. The cut-off of 167.6μg/μmol and 10.5 years were found as predictive factors of false positive Results.
Tobacco smoke interferes with immunochromatographic assay of urinary drug detection; therefore, all subjects must be questioned about their smoking status to avoid such false results during results interpretation.
Smoking is one of the main risk factors for cardiovascular disease (CVD). The mechanism(s) for the effects of smoking on CVD are not clearly understood; however, a number of atherogenic characteristics such as insulin resistance have been reported.
We aim to investigate the effects of cigarette smoking on insulin resistance and to determine the correlation between this parameter with smoking status characteristics.
This study was conducted on 138 nonsmokers and 162 smokers aged respectively 35.55±16.03 and 38.47±21.91 years. All subjects are not diabetics. Fasting glucose was determined by enzymatic methods and insulin by chemiluminescence method. Insulin resistance (IR) was estimated using the Homeostasis Model of Assessment equation: HOMA-IR = [fasting insulin (mU/L) × fasting glucose (mmol/L)] /22.5. IR was defined as the upper quartile of HOMA-IR. Values above 2.5 were taken as abnormal and reflect insulin resistance.
Results and discussion
Compared to non-smokers, smokers had significantly higher levels of fasting glucose, fasting insulin and HOMA-IR index. A statistically significant association was noted between the smoking status parameters, including both the number of cigarettes smoked/day and the duration of smoking, and fasting insulin levels as well for HOMA-IR index. Among smokers, we noted a positive correlation between HOMA-IR index and both plasma thiocyanates and urinary cotinine.
The findings show that smokers have a high risk to developing an insulin resistant, hyperinsulinaemic, compared with a matched group of non-smokers, and may help to explain the high risk of cardiovascular diseases in smokers.
Tobacco is a source of mineral elements that can affect human health in various ways, such as lithium, which is used as a psychiatric medication. Lithium salts are used as mood-stabilizing drugs and indicated in the treatment of manic-depressive psychosis.
Studying the lithium content in tobacco over the smokers’plasma content and evaluate the potential role of lithium in tobacco addiction.
A total of 18 different tobacco products (cigarettes, smokeless and water pipe tobacco) and 125 plasma samples (45 from smokers, 10 from ex-smokers and 70 from non-smokers) were collected to determinate the lithium content. Tobacco samples were digested with nitric acid and lithium concentration was measured by inductively coupled plasma-optical emission. The collected plasma samples were diluted 1/10 with a nitric acid solution and the lithium level was measured by inductively coupled plasma-mass spectrometry.
The average concentration of lithium in the cigarettes (16.59 ± 0.59 μg/g) was higher compared to those in the smokeless tobacco (8.39 ± 4.44 μg/g) and in the water pipe tobacco (6.13 ± 6.32 μg/g) but with no significant difference (P = 0.182). For plasma lithium levels, there was no significant difference (P = 0.186) between smokers and non-smokers (6.20 ± 6.24 vs. 4.98 ± 6.20 μg/g). However, a significant negative correlation was noted between plasma and the lithium content in tobacco products (r = –0.435; P = 0.04). The lithium plasma level was significantly and negatively correlated with the dependence score (r = –0.316; P = 0.031).
The correlation between plasmatic lithium and dependence score in smokers suggests that lithium would be involved in tobacco addiction probably through his regulating action of mood.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
Email your librarian or administrator to recommend adding this to your organisation's collection.